| Autor: |
Courty, Emilie, Besseiche, Adrien, Thi Thu Huong Do, Liboz, Alexandrine, Aguid, Fatima Mohamed, Quilichini, Evans, Buscato, Melissa, Gourdy, Pierre, Gautier, Jean-François, Riveline, Jean-Pierre, Haumaitre, Cécile, Buyse, Marion, Fève, Bruno, Guillemain, Ghislaine, Blondeau, Bertrand, Do, Thi Thu Huong |
| Předmět: |
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| Zdroj: |
Diabetes; Jan2019, Vol. 68 Issue 1, p95-108, 14p |
| Abstrakt: |
Both type 1 and type 2 diabetes are characterized by deficient insulin secretion and decreased β-cell mass. Thus, regenerative strategies to increase β-cell mass need to be developed. To characterize mechanisms of β-cell plasticity, we studied a model of severe insulin resistance in the adult mouse and defined how β-cells adapt. Chronic corticosterone (CORT) treatment was given to adult mice and led to rapid insulin resistance and adaptive increased insulin secretion. Adaptive and massive increase of β-cell mass was observed during treatment up to 8 weeks. β-Cell mass increase was partially reversible upon treatment cessation and reinduced upon subsequent treatment. β-Cell neogenesis was suggested by an increased number of islets, mainly close to ducts, and increased Sox9 and Ngn3 mRNA levels in islets, but lineage-tracing experiments revealed that neoformed β-cells did not derive from Sox9- or Ngn3-expressing cells. CORT treatment after β-cell depletion partially restored β-cells. Finally, β-cell neogenesis was shown to be indirectly stimulated by CORT because serum from CORT-treated mice increased β-cell differentiation in in vitro cultures of pancreatic buds. Altogether, the results present a novel model of β-cell neogenesis in the adult mouse and identify the presence of neogenic factors in the serum of CORT-treated mice. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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